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What causes aging of our body? Four complementary studies, including one from Northwestern Medicine, reached the same conclusion, long genes.
In a recent study, scientists describe their results and how they contribute to existing knowledge about aging.
“Tall genes that become less active with age may be a central cause of aging in our bodies,” said co-corresponding author Thomas Stoegger, MD, assistant professor of medicine in pulmonary and critical care at Northwestern University Feinberg School of Medicine. ” Potoxnak Longevity Institute. “Our discovery advances the field by identifying a single phenomenon that combines most of the existing knowledge about aging and makes this underlying phenomenon measurable.”
The paper, which highlights the shared findings of four international research groups, was published March 21 in Trends in Genetics. The group are the first to conclude that most aspects of biological aging are related to gene length.
Conditions known to accelerate aging reduce the activity of tall genes. This includes oxidative stress and UV radiation. Conditions known to slow aging, such as calorie restriction, increase the activity of tall genes. In addition, genes that are too short or too long encode for cellular processes known to change with aging, such as cellular energy production, protein synthesis, and transmission of nerve signals.
Also read: Here’s why we age?
“Gene regulation is one of the most central processes of life, and our four studies explain why the activity of long genes specifically changes with aging,” Stoerger said. “In addition to aging, we show that the same thing occurs in patients with the age-related disease Alzheimer’s disease. Our findings help us reconsider the causes of neurodegenerative diseases such as Alzheimer’s disease. Because genes involved in nerve function become abnormal are formally longer, we hypothesize that the decreased activity of long gene cells fails to produce sufficient biomaterial to properly maintain neural function.”
Scientists report that aging is a physiological phenomenon related to gene length, not the specific genes involved or the function of those genes. The original findings were based on a combination of molecular data from experiments in humans, mice, rats, killifish, C. elegans, D. melanogaster, and mice. Earlier scientific research tried to identify specific genes responsible for aging. This new approach differs from prevalent biological approaches that study the effects of single genes.
Longer genes simply have more potential sites that can be damaged. Scientists compare it to a road trip – the longer the trip, the greater the chance of something going wrong. And because the physiological roles of some types of cells depend on genes that last longer than those of other types of cells, some types of cells are more likely to be affected by the DNA damage that accumulates as they age. It happens. During aging, genes are damaged as the DNA strands that contain genes break. This prevents cells from reading and activating the information contained in genes. The longer the gene, the more likely it is that at least one DNA damage site will be present and prevent activation of the gene.
Because nerve cells are known to rely particularly on long genes and are slow or non-dividing, they are particularly sensitive to this phenomenon. Several genes involved in brain loss during aging and linked to Alzheimer’s disease are unusually long. Pediatric cancer patients who are cured of DNA-damaging chemotherapy later suffer from premature aging, including neurodegeneration.
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